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Genome-Wide Analysis Identifies Germ-Line Risk Factors Associated with Canine Mammary Tumours
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology.
Evidensia Sodra Djursjukhuset, Stockholm, Sweden..
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Biochemistry and Microbiology. Univ Cambridge, Dept Vet Med, Cambridge, England..
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Biochemistry and Microbiology. Broad Inst MIT & Harvard, Cambridge, MA USA..
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2016 (English)In: PLoS Genetics, ISSN 1553-7390, E-ISSN 1553-7404, Vol. 12, no 5, e1006029Article in journal (Refereed) Published
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Abstract [en]

Canine mammary tumours (CMT) are the most common neoplasia in unspayed female dogs. CMTs are suitable naturally occurring models for human breast cancer and share many characteristics, indicating that the genetic causes could also be shared. We have performed a genome-wide association study (GWAS) in English Springer Spaniel dogs and identified a genome-wide significant locus on chromosome 11 (p(raw) = 5.6x10(-7), p(perm) = 0.019). The most associated haplotype spans a 446 kb region overlapping the CDK5RAP2 gene. The CDK5RAP2 protein has a function in cell cycle regulation and could potentially have an impact on response to chemotherapy treatment. Two additional loci, both on chromosome 27, were nominally associated (p(raw) = 1.97x10(-5) and p(raw) = 8.30x10(-6)). The three loci explain 28.1 +/- 10.0% of the phenotypic variation seen in the cohort, whereas the top ten associated regions account for 38.2 +/- 10.8% of the risk. Furthermore, the ten GWAS loci and regions with reduced genetic variability are significantly enriched for snoRNAs and tumour-associated antigen genes, suggesting a role for these genes in CMT development. We have identified several candidate genes associated with canine mammary tumours, including CDK5RAP2. Our findings enable further comparative studies to investigate the genes and pathways in human breast cancer patients.

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2016. Vol. 12, no 5, e1006029
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Genetics
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URN: urn:nbn:se:uu:diva-299514DOI: 10.1371/journal.pgen.1006029ISI: 000377197100030PubMedID: 27158822OAI: oai:DiVA.org:uu-299514DiVA: diva2:949665
Available from: 2016-07-22 Created: 2016-07-22 Last updated: 2017-11-28Bibliographically approved

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Melin, MalinArendt, MajaElvers, IngegerdMurén, EvaLindblad-Toh, Kerstin
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